Intro, Overall Divisions, and Staphylococcus
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- 5 groups of human infectious diseases
- Bacteria, fungi, protozoa, helminthes, viruses
- 3 Shapes of Bacteria
- Cocci, bacilli, spirochetes
- Arrangements of Cocci, ex.
- Diplococci: Neisseria, chains: Strep, clusters: Staph
- Smallest cell
- Mycoplasma
- Difference btw pro and euk cell wall
- Peptidoglycan
- General dif btw Gram – cell wall and Gram + cell wall
- -: Thin peptidoglycan layer, periplasmic space, outer membrane. + thick peptidoglycan layer, no outer membrane, (lipo)teichoic acid
- Dif btw lipo- and teichoic acid
- Lipo goes down to cell membrane, teichioic in wall
- Gram – cell wall characteristics
- Endotoxin LPS (Lipid A), periplasmic space (beta-lactamases), porins, O specific side chains
- How does Lipid A cause shock
- Released from dying bacteria, induces release of cytokines
- LPS is to gram – as ______ is to gram +
- Teichoic acid. (both can induce TSS)
- Parts of LPS and what they do
- Lipid A (induces fever/hypotension), O antigen: used for lab ID
- Functions of peptidoglycan
- Rigid support, protects against osmotic pressure
- Detailed morphology of Staph, strep, strep pneumoniae, Neisseria Bacillus, Salmonella, Corynebacterium, Fusobacterium, Vibrio, Borrelia, Treponena
- Clusters, chains, pairs w/pointed ends, kidney bean pair, rod w/square ends, rod w/rounded ends, club shaped, fusiform, comma-shaped, relaxed coil, tightly coiled
- Enzyme in peptidoglycan formation. Drug interaction?
- Transpeptidase, penicillins and cephalosporins inhibit this
- Describe mycobacterium cell wall and staining characteristics
- Mycolic acid à acid-fast stain. Don’t stain in gram stain
- What human enzyme kills bacteria, where is it, how does it work?
- Lysozymes: tears, secretions. Cleaves peptidoglycan
- Difference btw human/bact cell membrane
- Sterols in humans
- Gram + color, - color
- Purple. Pink.
- Steps in gram staining
- Thin film of suspension. Fix w/methanol. Flood w/crystal violet. Add iodine. Decolorize with alcohol. Flood w/counterstain. Rinse excess stain off
- Describe bacterial chromosome(s)
- Single, circular chromosome + plasmids
- What info do plasmids carry? Transposons?
- Plasmids: Antibiotic resistance, exotoxins, Transposons: antibiotic resistance genes
- What are plasmids?
- Extrachromosomal DNA
- Role of capsule, composition (w/exception)
- Antiphagocytic, polysaccharide, exception: anthrax (D-glutamic acid)
- Describe 2 fxns of pili
- Attachment, sex (conjugation)
- Describe fimbraie
- Adhesion protein
- Dif btw flagella and fimbraie/pili
- Flagella have directed movement
- How to flagella move. Define: monotrichous, amphitrichous, peritrichous, lophotrichous
- Rotate. One flagella, two. Flagella coming out all over. Tuft of flagella
- Describe motility of spriochete
- Flagella-like structure interwoven in spiral. Undulating motion
- What is glycocalyx. 2 kinds. What does it do?
- Gel like coating outside cell. Capsule and slime layer. Attaches bacteria to cells and prostheses
- Function of: inclusion bodies, nucleoid, ribosomes, mesosome
- Stored nutrients for later use. Location of bacterial chromosomes. Site of protein synthesis. Plasma membrane that fold into cytoplasm to increase surface area
- Why do spores form? How does form change? Killed by boiling? Any way to kill? Metabolically active?
- Lack of nutrients. Thick keratin-like coat. Survive for many years. No. Only at 121 degrees for at least 15 min. no.
- How do bacteria reproduce?
- Binary fission
- Fastest replicating bactera
- Clostridium perfringens
- #1 cause of diarrhea in US
- campylobactor
- Dif btw exotoxin and endotoxin
- Exotoxins are extraceullar proteins
- 4 phase of bacterial growth cycle. describe
- Lag (incorporation of nutrients), log (exponential growth), stationary (equil btw death and new bacteria), death
- Dif btw aerobes, anaerobes, facultatives, microaerophilic in terms of enzymes. What do enzymes do
- Aerobes and facultatives have superoxide dismutase and catalase (break down toxic products of O2 use)
- T or F bacteria are haploid
- T
- 2 processes to transfer DNA WITHIN bacteria
- Transposons and programmed rearrangements
- Medical importance of transposons. and programmed rearrangments
- Transposons: carry antibiotics resistance genes. Programmed rearrangments: evade immune system by putting new proteins (antigens on cell surface)
- 3 processes to transfer DNA btw bacteria
- Conjugation, transduction, transformation
- Describe conjugation. What is required?
- Donor sex pilus attaches to recipient. DNA moves along sex pilus. Requires F plasmid. At the end, both have a copy of transferred genetic material
- Describe transduction. What is lysogenic conversion
- DNA transferred via bacteriophage. If new protein made: lysogenic conversion
- Describe transformation. 2 ways it can happen.
- DNA itself transferred: via dying cells or experimentally
- Normal flora of skin
- S. epidermidis, Propionibacterium, Peptococcus, Candida
- How can candida cause disease
- IV drug use, gets into bloodstream. Endocarditis
- How can S. epidermidis cause disease
- It gets on prostethic devices: heart valves, joints
- Major normal flora of the nose
- Staph aureus
- 3 normal flora of throat and bacteria they inhibit
- Viridans strep (Strep pyogenes), Neisseria spp (N. meningitides), S. epidermidis (S. aureus)
- Normal flora of mouth – what problem do they cause.
- Viridans (Strep mutans): dental caries. Most common cause of subacute infective endocarditis. Anaerobes (Bacteriodes, Fusobacterium, Clostridium, Peptostreptococcus): cause lung abscess if aspirate
- Major site of bacteria in the body
- Colon
- What is the normal role of E. coli, aberrant role
- Normal GI flora, leading cause of UTI
- Normal flora of GI
- E. coli, Bacteriodes fragilis, Enterococcus faecalis, Pseudomanas aeruginosa
- What extraintestinal disease to these case: B. fragilis. E. faecalis. P. aeruginosa
- Peritonitis following trauma, appendicitis, diverticulitis. UTI, endocarditis. Various nosocomial infections
- Role of antibiotics in normal GI flora
- Can wipe out normal flora and allow rare bacteria to overrun (clostridium difficile)
- Major normal flora of GU tract, what happens when it’s suppressed
- Lactobacillus – keeps pH low.. Candida infection
- Bacteria on skin around GU tract
- S. saprophyticus
- Bacteria that can infect urine as it comes out urethra
- S. epidermidis, coliforms, diphtheroids, nonhemolytic streptococci
- Bacteria around urethra of women and uncircumcised men
- Mycobacterium smegmatis
- Female urethra can get bacteria from what area
- Fecal flora
- Define colonization resistance and give an example
- Normal flora take up receptor sites so pathogens can’t attach. Ex. Viridans strep on throat prevent GAS from binding
- Does E. coli produce a vitamin. If yes, what
- Yes, vitamin A
- Diseases caused by Staphlyococcus aureus
- Abscesses, various pyogenic infections (endocarditis, septic arthritis, osteomyelitis), food poisoning, TSS, nosocomial pneumonia, septicemia, surgical-wound infection. Meningitis, UTI, abscess formation of any organ
- T or F. gram + cocci are motile
- F
- T or F. gram + cocci do not form spores
- T
- Gram, catalase, coagulase status of staph spp
- Staph aureus: all +, S. epidermidis, saprophyticus: coagulase -
- What is catalase, why is it good for bacteria
- Degrades H2O2 into O2 and H2O, prevents peroxide from microbicidal activity of letting neutrophils kill
- What is coagulase
- Causes plasma to clot by activating prothrombin à thrombin
- T or F. s. aureus ferments mannitol
- T
- T of F. s. aureus is beta hemolytic
- T
- 90% of what bacteria have beta-lactamase. What is that?
- s. aureus. Degrades many penicillins
- How can s. aureus be resistant to beta-lactamase resistant penicillin
- Changes in penicillin binding protein
- 6 important cell wall components and antigens
- Protein A, teichoic acids, polysaccharide capsule, phage surface receptors, microcapsule, peptidoglycan
- Describe protein A
- Bind Fc portion of IgG, antiphagocytic
- Describe teichoic acid in staph
- Adherence to mucosal cells + play a role in septic shock
- Describe role of peptidoglycan in strep
- Endotoxin-like properties
- Role of staph as normal flora (3 kinds of staph)
- s. epidermidis: skin + hair follicles. S. aureus: nose. S. saprophyticus: skin around GU tract
- T or F. S. aureus disease thrives in heavily contaminated environment and immunocompromised people.
- T
- Typical lesion of s. aureus
- Abscess
- What happens to abscesses
- Central necrosis and drain to the outside
- Important predisposing factor in s. aureus infection
- Foreign bodies (sutures, IV catheters)
- 3 clinically important exotoxins in s. aureus
- Enterotoxin, toxic shock syndrome toxin, exfoliatin
- Describe what enterotoxin does and clinical manifestations
- Superantigen: release of IL-1 from macros, IL-2 from T helper cells. food poisoning. Prominent vomiting (signals enteric n.s. to stimulate vomiting center in brain) + watery, non-bloody diarrhea.
- Heat resistance, stomach acid, jejunum enzymes - reaction of enterotoxin
- Fairly heat resistant, resistant to stomach acid, jejunum enzymes
- Describe toxic shock syndrome toxin
- Causes toxic shock, esp in women w/tampon, nose tampon. Superantigen à IL-1, IL-2, TNF released
- Describe exfoliatin
- Causes “scalded skin syndromeâ€. Epidermolytic.
- What is alpha toxin?
- Kills leukocytes à skin necrosis and hemolysis.
- Name some virulence enzymes in s. aureus
- Coagulase, fibrinolysin, hyaluronidase, proteases, nucleases, lipases
- Proteins that disable host immunity in s. aureus
- Protein A, coagulase, hemolysins, penicillinase
- Proteins tunneling through tissue in s. aureus
- Hyaluronidase, staphylokinase, lipase
- Pathogenic mechanisms of s. aureus
- Toxins and inflamm due to multiplying in tissues
- T of F. All spp of staph produce exotoxin
- F: S. epidermidis and S. saprophyticus don’t – also means no food poisoning or septic shock
- What are 2 divisions of clinical manifestations of s. aureus
- Pyogenic and toxin-mediated
- Pyogenic diseases of s. aureus
- Skin infections, septicemia, endocarditis (esp R. sided tricuspid in IV drug uses), osteomyelitis, arthritis, postsurgical wound infection, pneumonia, abscesses
- What does staph pneumonia often lead to?
- Empyema and lung abscess
- Toxin-mediated diseases of s. aureus
- Food poisoning – ingest enterotoxin. TSS, scalded skin syndrome
- Clinical manifestation of TSS
- Hypotension; macular, sunburn like rash, 3+ organ involvement
- Clinical manifestation of scalded skin syndrome. Age group often affected
- Fever, large bullae, erythematous rash, skin slough, serous fluid exudes, electrolyte imbalance, skin and hair loss. Recovery takes 7-10 d. young children
- Diseases caused by S. epidermidis
- Infect protheses, neonatal sepsis, peritonitis in renal pts with catheter, cerebrospinal fluid shunt infection
- What is the most common cause of cerebrospinal fluid shunt infection
- s. epidermidis
- What determines if S. epidermidis adheres well to prostheses?
- Presence of glycocalyx
- Diseases caused by S. saprophyticus
- UTI.
- Top two causes of community acquired UTI
- E. coli, S. saprophyticus
- Lab Dx: gram, culture, coagulase, mannitol
- +. golden-yellow, beta hemolytic. +. +
- Lab dx: culture of coagulase - staph
- White colonies, non hemolytic
- Role of novobiocin in staph
- s. epidermidis sensitive, s. saprophyticus not
- Bacteriophages and lab dx for staph
- Staph can be divided into groups based on their lysis
- T or F. 90% of s. aures resistant to penicillin
- T
- Why are most s. aureus resistant to penicillin?
- Contain beta lactamase
- what meds are some s. aureus resistant to?
- Penicillin, methicillin, nafcillin, partial vancomycin
- Tx of staph toxic shock syndrome
- Correct hypotension w/fluids. Pressor drugs, inotropes, beta lactamase resitant penicillin.
- Topical antibiotic for staph
- Mupirocin
- Definition of tolerance
- Bacteria can’t grow but not killed by med
- Treatment of abscesss
- Surgical drainage
- T or F. S. epidermidis is highly resistant to antibiotics
- T. use vancomycin +/- another drug. Remove prosthesis
- Prevention of staph infections
- Hygiene!!!, remove shedders from high-risk areas, peri-op antibiotics
- Are viruses cells
- Y
- What is the only group that has a nucleus
- Eurkaryotes
- Which group has DNA or RNA
- Viruses
- Describe chromatin of euk, arch, pro and viruses
- Many, complexed w/histones. Single loop. single, circular chromatin + plasmids, none
- Describe ribosomes of euk, arch, pro, viruses
- 80S, 70S, 70S, none
- Which group has mitochondria
- Euks only
- Outer surface of euk, arch, pro, viruses
- Euk: cell membrane w/sterols. Chitin wall, ergosterol. Arc: glycerol/isoprene derivatives. Pro: peptidoglycan + cell membrane, maybe capsule. Viruses: naked protein capsid + lipoprotein envelope
- Motility: euk, arc, pro, viruses
- Flagella, cilia, pseudopods. Flagella, flagella. None
- Difference btw bacteriostatic and bactericidal
- Inhibits bacterial growth (host defenses need to kill). Kill bacteria.
- Reasons for antibiotic failure
- Delay in dx, tx. Wrong dx. Errors in susceptibility testing. Inadequate concentration of bacteria at infection site. other factors at site. immunocompromised pt. superinfection. resistance.
- How can you distinguish btw N. gonorrhea and N. meningitidis
- Fermentation of glucose or maltose
- How you distinguish E. coli from Shigella and Salmonella
- Fermentation of lactose